Spencer C. Knox, MD

Internal Medicine Resident Physician, PGY-3

Tag: diagnosis

Inflammatory Bowel Disease (IBD)

IBD is an important clinical entity, made up of two idiopathic processes:  Crohn Disease (CD) and Ulcerative Colitis (UC).  Risk factors involve both genetic (higher incidence in identical twins) and environmental sources.  Cigarette smoking = risk factor for CD, protective for UC.  Northern populations see higher rates of IBD.  Note:  may utilize ESR and CRP levels to monitor response to therapy.  Finally, patients with chronic colitis ( > 8-10 years in duration) need surveillance colonoscopy q1-2 years to evaluate for colon cancer, as these IBD patients are at increased risk.

Extraintestinal Manifestations of IBD

  • Occur in 10% of patients with known IBD, usually present before GI symptoms.
  • Top signs/symptoms:
    • Oral aphthous ulcers, back pain (AS or sacroiliitis), and joint pain.
  • Others include ocular (uveitis, scleritis) and dermatologic (erythema nodosum and pyoderma gangrenosum).
  • Liver = primary sclerosing cholangitis (PSC)

Ulcerative Colitis (UC)

  • “Bloody UC!”
  • Clinically
    • Patient complains of bloody diarrhea and abdominal pain; constipation if distal (rectal muscle tone increase).
    • Depending of where inflammation is, symptoms may change – typically inflammation arises in distal colon, moves its way up (not always)
      • Proctitis – rectal lesions only
      • Left-sided colitis – inflammation in the anatomical left colon (to splenic flexure)
      • Pancolitis – involving the entire large intestine (colon).
    • Physical exam:  normal to severe (tachycardia, fever, dehydration, pallor; even hypoactive bowel sounds and rebound tenderness which may suggest bowel perforation or megacolon).
    • Labwork:  derangements on CBC, low albumin, BMP anomalies (electrolytes).
  • Diagnosis
    • Colonoscopy with biopsy
      • Mucosal lining swelling and erythema, loss of vasculature; fragility, granularity, ulcers, hemorrhage.
      • Pathology:  abnormal crypt anatomy.
    • Inflammation moves in continuous proximal fashion starting at rectum – 50% will have pancolitis at presentation!
    • “Back wash ileitis” – pancolitis patients who also have disease in the ileum.
  • Treatment of UC
    • 1st line = 5-ASA drugs
      • Used for inducing remission and maintenance therapy
      • 5-ASA delivered to colon
      • Mesalamine – goes to small and large intestines (prepared specifically for targeted delivery)
    • Severe UC = Oral Glucocorticoids
      • Prednisone 40-60 mg/day
      • Budesonide MMX (high first pass metabolism reduces systemic effects)
    • Maintenance therapy:
      • If glucocorticoid-responsive, transition to:
        • AZA or 6-MP (test for TPMT level – if low level, patient is at risk for toxicity as this inactivates 6-MP.
      • If non-responsive to glucocorticoids, transition to:
        • Biologics:  cyclosporine or anti-TNF antibodies (infliximab, adalimumab, golimumab)


Crohn Disease (CD)

  • Clinically
    • C/C diarrhea, weight loss, abdominal discomfort.
    • LESS likely to report bleeding/fever.
    • Distribution:
      • 30% small-bowel only (belly pain), 40% ileocolonic disease (RLQ pain), 25% colonic disease only (bleeding per rectum, fistula formation), 5% upper GI or perianal (urgency and/or tenesmus)
  • Pathophysiology
    • Transmural inflammation, leading to fistula formation!  More infections.
  • Diagnosis
    • Colonoscopy with biopsy
      • Superficial to deep ulcers, may combine to form “cobblestone” appearance. (Crohn Cobblestone) – rectum is spared.
      • Skip lesions (regions of normal tissue)
      • Ileum inflammation is typical – required to biopsy this area!
      • Pathology:  patchy transmural inflammation
    • CT or MR enterography, video capsule endoscopy are sometimes useful.
  • Treatment of Crohn Disease
    • Induction is typically with glucocorticoids (prednisone, or budesonide if ileocolonic)
    • Maintenance:
      • Steroid-responsive – Transition from prednisone to immunomodulator (AZA, 6-MP, or methotrexate)
      • Very severe disease – BIOLOGIC anti-TNF, can close fistulas and are pregnancy category B
        • Infliximab, adalimumab, certolizumab.
    •  For test-taking purposes:
      • Natalizumab is a mab that can cause PML (JC Virus).
      • Vedolizumab – leukocyte trafficking antagonist that does not work in brain.


  • ACP MKSAP 17:  Gastroenterology and Hepatology, pgs. 37-41
  • Image source:  https://www.pinterest.com/kimerydavis/ulcerative-colitis/

Heart Failure Pathophysiology and Diagnosis

  • In an average healthy person, normal LV ejection fraction (LVEF):  >50%
  • Roughly 50% of those with heart failure have reduced left ventricular (LV) function (HFrEF)
    • Heart cannot squeeze/contract properly, and then progressively dilates.
  • The other 50% have preserved (normal contraction) LV function (HFpEF)
    • Cannot relax properly, leading to high diastolic (filling) pressures.
  • New heart failure – work patient up for ischemic disease (CAD) and ACS
    • Coronary Artery Disease causes 67% of heart failure!  #1 cause of heart failure
  • Symptomatic hypotension and kidney failure can be due to cardiac output failure.  Organs simply do not have sufficient blood to perfuse and stay alive.
  • Etiology of HFrEF
    • Hypertension
    • CAD
    • Myocarditis
    • Drugs – cyclophosphamide, doxorubicin, trastuzumab
    • Toxins – EtOH, cocaine, cobalt/lead, amphetamines
    • Systemic disease – hypo- or hyperthyroidism, HIV, SLE, Neuromuscular disease (Duchenne & Becker muscular dystrophy), scleroderma
    • Idiopathic (unknown cause)
  • Etiology of HFpEF
    • Hypertension
    • CAD
    • Infiltrative – amyloidosis & hemochromatosis (check ferritin)
  • Clinical signs and symptoms
    • Shortness of breath either with exertion or at rest
    • Orthopnea (shortness of breath lying flat on one’s back)
    • Paroxysmal nocturnal dyspnea (sudden bouts of shortness of breath and cough during the night/sleep hours)
    • Peripheral edema (swelling of feet/legs)
    • Decompensated signs/symptoms
      • More pillows at nighttime
      • Can’t walk up as many stairs before getting short of breath
      • Increased belly size, anorexia, nausea (gut edema)
  • Patients must weigh themselves daily, call the office if interval change.
  • History and physical
  • Paroxysmal nocturnal dyspnea leads to >2x increase in likelihood of HF
  • S3 confers 11x greater chance of HF.
  • If no dyspnea on exertion or crackles on lung exam, HF less likely.
  • BNP level – use when cause not clear.  If elevated, dyspnea is due to heart failure!  If not, consider other lungs as cause.
    • BNP level increases with age and bad kidneys
    • BNP level decreases with high BMI.
  • 12-lead EKG
    • Rule out MI, tachycardia, LV hypertrophy
  • CXR
  • Labs – BMP, CBC, UA, LFTs, lipid panel, TSH
Workup to Find A Cause
  • Must think of Ischemia first –
    • Serial EKGs and troponin levels to evaluate for NSTEMI/STEMI.
    • Routine investigation via stress or cath no longer part of routine workup for new HF patients.
    • However, if chest pain/pressure and/or risk factors are present –> proceed to cardiac cath.
  • Echocardiogram is most important test in HF.
    • “Wall motion abnormalities” is a clue to CAD or MI.
    • Assesses valvular anatomy and function
    • Left ventricular end-diastolic dimension:  can aid in telling how chronic the condition is and prognosis.
      • If DILATED w/acute symptoms –> chronic disease process.
      • If small LV –> better shot at recovery.
  • Cardiac magnetic resonance (CMR)
    • Looks for wall motion abnormalities, perfusion, and VIABILITY of tissue.
    • If thinking fibrosis, infiltration (amyloid/sarcoid), or iron deposition.

ACP MKSAP 17:  Cardiovascular Medicine, pp. 32-34

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